True or false? Terbinafinea) acts on fungal cell wallb) is used in the treatment of dermatophytosesc) is not available for oral used) is used in the treatment of mucormycosise) is used in the treatment of infection with Pneumocystis jirovecii
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Terbinafine - True or False
a) Acts on fungal cell wall - FALSE
Terbinafine is a synthetic allylamine that acts on the fungal cell membrane, not the cell wall. It inhibits squalene epoxidase, the enzyme that converts squalene to ergosterol. This leads to accumulation of toxic squalene intermediates and depletion of ergosterol in the fungal membrane, causing cell death.
(Goodman & Gilman's, p. 1224; Lippincott Pharmacology, p. 1098)
Note: Cell wall-active antifungals are the echinocandins (caspofungin, micafungin, anidulafungin), which inhibit beta-1,3-glucan synthase.
b) Is used in the treatment of dermatophytoses - TRUE
Terbinafine is the drug of choice for dermatophyte infections (tinea capitis, tinea unguium/onychomycosis, tinea corporis, tinea pedis, tinea cruris). It is fungicidal against dermatophytes (Trichophyton, Microsporum, Epidermophyton) and is superior to griseofulvin and itraconazole for nail infections.
(Fitzpatrick's Dermatology; Lippincott Pharmacology, p. 1098)
c) Is not available for oral use - FALSE
Terbinafine IS available orally as a 250 mg tablet (once daily for adults). It is also available topically (1% cream, gel, spray). Oral bioavailability is ~40% due to first-pass metabolism; the drug accumulates in skin, nails, and adipose tissue with a terminal half-life of 200-400 hours.
(Goodman & Gilman's, p. 1224; Lippincott Pharmacology, p. 1099)
d) Is used in the treatment of mucormycosis - FALSE
Terbinafine has no meaningful activity against Mucorales (the cause of mucormycosis). Treatment of mucormycosis requires liposomal amphotericin B (first-line), with isavuconazole or posaconazole as alternatives. Terbinafine penetrates poorly into deep tissues and is not used for systemic or invasive fungal infections.
(Harrison's 22E; Goodman & Gilman's)
e) Is used in the treatment of infection with Pneumocystis jirovecii - FALSE
Terbinafine has no activity against Pneumocystis jirovecii. Treatment of P. jirovecii pneumonia (PCP) uses TMP-SMX (co-trimoxazole) as first-line, with alternatives including pentamidine, atovaquone, or dapsone + trimethoprim. Goodman & Gilman's places the "Agents Active Against Pneumocystis" in a completely separate section from terbinafine.
(Goodman & Gilman's, p. 1224-1215)
Summary Table
| Statement | Answer | Reason |
|---|---|---|
| a) Acts on fungal cell wall | FALSE | Acts on cell membrane via squalene epoxidase inhibition |
| b) Used for dermatophytoses | TRUE | Drug of choice for tinea/onychomycosis |
| c) Not available for oral use | FALSE | Available as 250 mg oral tablet |
| d) Used for mucormycosis | FALSE | No activity; use amphotericin B |
| e) Used for P. jirovecii | FALSE | No activity; use TMP-SMX |
Fluconazolea) acts on the fungal cell wallb) cannot be given orallyc) penetrates into the CSF welld) is useful in the treatment of Cryptococcus neoformanse) is indicated in resistant candida infection
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Fluconazole - True or False
a) Acts on the fungal cell wall - FALSE
Fluconazole is a bis-triazole that acts on the fungal cell membrane, not the cell wall. It inhibits lanosterol 14α-demethylase (a fungal CYP51 enzyme), blocking the conversion of lanosterol to ergosterol - the key structural component of the fungal membrane. This depletes ergosterol and allows toxic methylated sterol intermediates to accumulate.
(Fitzpatrick's Dermatology; Goodman & Gilman's)
Reminder: Cell wall-active agents = echinocandins (inhibit β-1,3-glucan synthase).
b) Cannot be given orally - FALSE
Fluconazole has excellent oral bioavailability of ~90% - nearly identical to the intravenous route. Its pharmacokinetics are linear, predictable, and not affected by gastric acidity or food intake. It is available as tablets (150 mg capsules), oral suspension, and IV solution.
(Fitzpatrick's Dermatology, p. 4408)
c) Penetrates into the CSF well - TRUE
This is one of fluconazole's key distinguishing features among antifungals. Because it has low protein binding, it achieves CSF concentrations of ~70-80% of plasma levels - far superior to most other antifungals (e.g., itraconazole has negligible CSF penetration). This property makes it valuable in CNS fungal infections.
(Fitzpatrick's Dermatology; Harrison's 22E; K.J. Lee's Essential Otolaryngology)
d) Is useful in the treatment of Cryptococcus neoformans - TRUE
Fluconazole is used in consolidation and maintenance (suppression) therapy for cryptococcal meningitis. The standard regimen is:
- Induction: Amphotericin B + flucytosine (2 weeks)
- Consolidation: Fluconazole 400 mg/day (8 weeks)
- Maintenance: Fluconazole 200 mg/day (to prevent relapse)
Its excellent CSF penetration makes it ideal for this role.
(Harrison's 22E; Goodman & Gilman's)
e) Is indicated in resistant Candida infection - FALSE
Fluconazole is NOT indicated in resistant Candida - in fact, certain Candida species are intrinsically resistant to it:
| Species | Fluconazole Susceptibility |
|---|---|
| C. albicans | Susceptible |
| C. krusei (now Pichia kudriavzevii) | Intrinsically resistant |
| C. auris | Intrinsically resistant |
| C. glabrata (now Nakaseomyces glabrata) | ~30% resistant / dose-dependent |
| C. lusitaniae | Susceptible but varies |
For resistant Candida, echinocandins (caspofungin, micafungin) or amphotericin B are used instead.
(Quick Compendium of Clinical Pathology 5th ed.; Medical Microbiology 9e; Jawetz Microbiology)
Summary Table
| Statement | Answer | Key Point |
|---|---|---|
| a) Acts on fungal cell wall | FALSE | Acts on cell membrane - inhibits lanosterol 14α-demethylase |
| b) Cannot be given orally | FALSE | ~90% oral bioavailability |
| c) Penetrates CSF well | TRUE | ~70-80% of plasma levels; low protein binding |
| d) Useful for C. neoformans | TRUE | Consolidation/maintenance in cryptococcal meningitis |
| e) Indicated in resistant Candida | FALSE | C. krusei and C. auris are intrinsically resistant to it |
Fluconazolea) has good oral bioavailabilityb) is nephrotoxicc) is the first choice antimicrobial for the treatment of resistant candidiasisd) covers Cryptococcus neoformanse) can be used in the treatment of pneumocystosis
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All sources confirmed. Here is the complete answer:
Fluconazole (Second Set) - True or False
a) Has good oral bioavailability - TRUE
Fluconazole has ~90% oral bioavailability, essentially equivalent to the IV route. Unlike most other antifungals (e.g., itraconazole capsules, which need food and acid for absorption), fluconazole absorption is independent of gastric acidity and food intake. It also has low plasma protein binding, a long half-life of 25-30 hours, and excellent tissue distribution including the CSF.
(Fitzpatrick's Dermatology, p. 4408)
b) Is nephrotoxic - FALSE
Fluconazole is not nephrotoxic. Its adverse effect profile includes GI symptoms (nausea, dyspepsia, diarrhea), headache, QT prolongation, and rarely severe skin reactions (SJS/TEN) - but kidney toxicity is not among them. Fluconazole is actually eliminated primarily by the kidneys, so dose adjustment is needed in renal impairment - but this is not because it damages the kidneys.
The classic nephrotoxic antifungal is amphotericin B (conventional deoxycholate formulation), which causes acute kidney injury in up to one-third of patients.
(Fitzpatrick's Dermatology, p. 4416; Comprehensive Clinical Nephrology 7th ed.)
c) Is the first-choice antimicrobial for resistant candidiasis - FALSE
This is the opposite of the truth. Fluconazole is NOT used for resistant Candida - it is avoided precisely because resistance is the problem. The first-line agents for resistant or invasive candidiasis are:
- Echinocandins (caspofungin, micafungin, anidulafungin) - first-line for invasive candidiasis and candidemia, active against C. krusei, C. glabrata, and C. auris
- Liposomal amphotericin B - alternative when echinocandins fail
(Red Book 2021; Fitzpatrick's Dermatology; Lippincott Pharmacology)
d) Covers Cryptococcus neoformans - TRUE
Fluconazole has good activity against C. neoformans and is a standard part of cryptococcal meningitis treatment:
- Induction (2 wks): Amphotericin B + flucytosine
- Consolidation (8 wks): Fluconazole 400 mg/day
- Maintenance/suppression: Fluconazole 200 mg/day (prevents relapse, especially in HIV)
Its excellent CNS penetration makes it ideal for this purpose.
(Harrison's 22E; Goodman & Gilman's)
e) Can be used in the treatment of pneumocystosis - FALSE
Fluconazole has no activity against Pneumocystis jirovecii (PCP). The fungal cell wall and membrane of P. jirovecii are structurally atypical - it lacks ergosterol, making azoles ineffective against it.
Treatment of PCP:
| Setting | Drug |
|---|---|
| First-line | TMP-SMX (trimethoprim-sulfamethoxazole) |
| Alternatives | Pentamidine, atovaquone, dapsone + trimethoprim |
| Prophylaxis | TMP-SMX, dapsone, aerosolized pentamidine |
(Harrison's 22E)
Summary Table
| Statement | Answer | Key Point |
|---|---|---|
| a) Good oral bioavailability | TRUE | ~90%, independent of food/gastric acid |
| b) Is nephrotoxic | FALSE | Not nephrotoxic; amphotericin B is the nephrotoxic antifungal |
| c) First choice for resistant candidiasis | FALSE | Echinocandins are first-line for resistant/invasive candidiasis |
| d) Covers C. neoformans | TRUE | Consolidation & maintenance therapy for cryptococcal meningitis |
| e) Used for pneumocystosis | FALSE | P. jirovecii lacks ergosterol; TMP-SMX is first-line |
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